CoChat
Sign Up
Cited by 20

The DOI matches its Crossref record; 18 of the 18 references it cites were found in a registry or an index.

Development of MAPT S305 mutation human iPSC lines exhibiting elevated 4R tau expression and functional alterations in neurons and astrocytes

Bowles, Kathryn R., Pedicone, Chiara, Pugh, Derian A., Oja, Laura-Maria, Sousa, Filipa H., Keavey, Lois K., Fulton-Howard, Brian, Weitzman, Sarah A., Liu, Yiyuan, Chen, Jonathan L., Disney, Matthew D., Goate, Alison M.·2024·Cell Reports
DOI 10.1016/j.celrep.2024.115013PMC PMC13478741
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.celrep.2024.115013

Cites

18 of 18 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Modeling 4R tauopathy in human neurons and astrocytes has been implemented, providing a unique platform to investigate the molecular and cellular mechanisms underlying the development and progression of tau pathology with both 3R- and 4R-tau isoforms as seen in FTLD and AD patients.

    “Recently, modeling 4 R tauopathy in human neurons53,83,110,111 and astrocytes110 has been implemented, which provides a unique platform to investigate the molecular and cellular mechanisms underlying the development and progression of tau pathology with both 3R- and 4R-tau isoforms as seen in FTLD and AD patients.”

    From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [110]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 78

  1. Trabzuni, 2012, MAPT expression and splicing is differentially regulated by brain region: Relation to genotype and implication for tauopathies, Hum. Mol. Genet., 21, 4094, 10.1093/hmg/dds238 · DOI · Paper page
  2. Beevers, 2017, MAPT Genetic Variation and Neuronal Maturity Alter Isoform Expression Affecting Axonal Transport in iPSC-Derived Dopamine Neurons, Stem Cell Rep., 9, 587, 10.1016/j.stemcr.2017.06.005 · DOI
  3. Hefti, 2018, High-resolution temporal and regional mapping of MAPT expression and splicing in human brain development, PLoS One, 13, e01957711, 10.1371/journal.pone.0195771 · DOI
  4. Rösler, 2019, Four-repeat tauopathies, Prog. Neurobiol., 180, 10.1016/j.pneurobio.2019.101644 · DOI
  5. Iovino, 2015, Early maturation and distinct tau pathology in induced pluripotent stem cell-derived neurons from patients with MAPT mutations, Brain, 138, 3345, 10.1093/brain/awv222 · DOI · Paper page
  6. Silva, 2016, Human iPSC-Derived Neuronal Model of Tau-A152T Frontotemporal Dementia Reveals Tau-Mediated Mechanisms of Neuronal Vulnerability, Stem Cell Rep., 7, 325, 10.1016/j.stemcr.2016.08.001 · DOI · Paper page
  7. Lovejoy, 2020, Engineered Cerebral Organoids Recapitulate Adult Tau Expression and Disease-relevant Changes in Tau Splicing, Alzheimers Dement, 16
  8. Mahali, 2021, Defective proteostasis in patient-derived iPSC astrocytes and neurons carrying a MAPT IVS10+16 mutation, Alzheimers Dement, 17, 10.1002/alz.058727 · DOI
  9. Minaya, 2023, Conserved gene signatures shared among MAPT mutations reveal defects in calcium signaling, Front. Mol. Biosci., 10, 1051494, 10.3389/fmolb.2023.1051494 · DOI
  10. Jiang, 2018, Integrative system biology analyses of CRISPR-edited iPSC-derived neurons and human brains reveal deficiencies of presynaptic signaling in FTLD and PSP, Transl. Psychiatry, 8, 265, 10.1038/s41398-018-0319-z · DOI · Paper page
  11. Nakamura, 2019, Pathological Progression Induced by the Frontotemporal Dementia-Associated R406W Tau Mutation in Patient-Derived iPSCs, Stem Cell Rep., 13, 684, 10.1016/j.stemcr.2019.08.011 · DOI
  12. Silva, 2020, Prolonged tau clearance and stress vulnerability rescue by pharmacological activation of autophagy in tauopathy neurons, Nat. Commun., 11, 3258, 10.1038/s41467-020-16984-1 · DOI · Paper page
  13. Wray, 2017, Modeling tau pathology in human stem cell derived neurons, Brain Pathol., 27, 525, 10.1111/bpa.12521 · DOI
  14. Kopach, 2021, Genetically engineered MAPT 10+16 mutation causes pathophysiological excitability of human iPSC-derived neurons related to 4R tau-induced dementia, Cell Death Dis., 12, 10.1038/s41419-021-04007-w · DOI · Paper page
  15. Handel, 2016, Assessing similarity to primary tissue and cortical layer identity in induced pluripotent stem cell-derived cortical neurons through single-cell transcriptomics, Hum. Mol. Genet., 25, 989, 10.1093/hmg/ddv637 · DOI
  16. Sposito, 2015, Developmental regulation of tau splicing is disrupted in stem cell-derived neurons from frontotemporal dementia patients with the 10 + 16 splice-site mutation in MAPT, Hum. Mol. Genet., 24, 5260, 10.1093/hmg/ddv246 · DOI · Paper page
  17. Verheyen, 2018, Genetically Engineered iPSC-Derived FTDP-17 MAPT Neurons Display Mutation-Specific Neurodegenerative and Neurodevelopmental Phenotypes, Stem Cell Rep., 11, 363, 10.1016/j.stemcr.2018.06.022 · DOI · Paper page
  18. Miguel, 2019, Detection of all adult Tau isoforms in a 3D culture model of iPSC-derived neurons, Stem Cell Res., 40, 10.1016/j.scr.2019.101541 · DOI
  19. Habekost, 2021, Directly Reprogrammed Neurons Express MAPT and APP Splice Variants Pertinent to Ageing and Neurodegeneration, Mol. Neurobiol., 58, 2075, 10.1007/s12035-020-02258-w · DOI
  20. Iijima, 1999, A distinct familial presenile dementia with a novel missense mutation in the tau gene, Neuroreport, 10, 497, 10.1097/00001756-199902250-00010 · DOI
  21. Kovacs, 2008, MAPT S305I mutation: Implications for argyrophilic grain disease, Acta Neuropathol., 116, 103, 10.1007/s00401-007-0322-6 · DOI
  22. Stanford, 2000, Progressive supranuclear palsy pathology caused by a novel silent mutation in exon 10 of the tau gene Expansion of the disease phenotype caused by tau gene mutations, Brain, 123 ( Pt 5), 880, 10.1093/brain/123.5.880 · DOI · Paper page
  23. Skoglund, 2008, The tau S305S mutation causes frontotemporal dementia with parkinsonism, Eur. J. Neurol., 15, 156, 10.1111/j.1468-1331.2007.02017.x · DOI
  24. Chen, 2019, The RNA encoding the microtubule-associated protein tau has extensive structure that affects its biology, PLoS One, 14, e0219210, 10.1371/journal.pone.0219210 · DOI
  25. Reuter, 2010, RNAstructure: software for RNA secondary structure prediction and analysis, BMC Bioinf., 11, 129, 10.1186/1471-2105-11-129 · DOI
  26. Spires-Jones, 2014, The intersection of amyloid beta and tau at synapses in Alzheimer’s disease, Neuron, 82, 756, 10.1016/j.neuron.2014.05.004 · DOI · Paper page
  27. Tracy, 2022, Tau interactome maps synaptic and mitochondrial processes associated with neurodegeneration, Cell, 185, 712, 10.1016/j.cell.2021.12.041 · DOI
  28. Mondragón-Rodríguez, 2012, Interaction of endogenous tau protein with synaptic proteins is regulated by N-methyl-D-aspartate receptor-dependent tau phosphorylation, J. Biol. Chem., 287, 32040, 10.1074/jbc.M112.401240 · DOI · Paper page
  29. Sahara, 2014, Biochemical distribution of tau protein in synaptosomal fraction of transgenic mice expressing human p301l tau, Front. Neurol., 5, 26, 10.3389/fneur.2014.00026 · DOI
  30. Wu, 2021, The role of pathological tau in synaptic dysfunction in Alzheimer’s diseases, Transl. Neurodegener., 10, 45, 10.1186/s40035-021-00270-1 · DOI · Paper page
  31. Radovani, 2022, N-Glycosylation and Inflammation; the Not-So-Sweet Relation, Front. Immunol., 13, 893365, 10.3389/fimmu.2022.893365 · DOI
  32. Chacko, 2014, The Bioenergetic Health Index: a new concept in mitochondrial translational research, Clin. Sci., 127, 367, 10.1042/CS20140101 · DOI
  33. Guzman-Martinez, 2019, Neuroinflammation as a common feature of neurodegenerative disorders, Front. Pharmacol., 10, 1008, 10.3389/fphar.2019.01008 · DOI · Paper page
  34. Esteras, 2017, Mitochondrial hyperpolarization in iPSC-derived neurons from patients of FTDP-17 with 10+16 MAPT mutation leads to oxidative stress and neurodegeneration, Redox Biol., 12, 410, 10.1016/j.redox.2017.03.008 · DOI
  35. Haque, 2019, Crosstalk between oxidative stress and tauopathy, Int. J. Mol. Sci., 20, 10.3390/ijms20081959 · DOI
  36. Ezerskiy, 2022, Astrocytic 4R tau expression drives astrocyte reactivity and dysfunction, JCI Insight, 7, 10.1172/jci.insight.152012 · DOI
  37. Sidoryk-Wegrzynowicz, 2017, Astrocytes in mouse models of tauopathies acquire early deficits and lose neurosupportive functions, Acta Neuropathol. Commun., 5, 89, 10.1186/s40478-017-0478-9 · DOI
  38. Cisternas, 2022, The reduction of astrocytic tau prevents amyloid-β-induced synaptotoxicity, Brain Commun., 4, 10.1093/braincomms/fcac235 · DOI
  39. Fischer, 2020, Resurrecting the Mysteries of Big Tau, Trends Neurosci., 43, 493, 10.1016/j.tins.2020.04.007 · DOI
  40. Ferrer, 2018, Astrogliopathy in Tauopathies, Neuroglia, 1, 126, 10.3390/neuroglia1010010 · DOI
  41. Bowles, 2022, Dysregulated coordination of MAPT exon 2 and exon 10 splicing underlies different tau pathologies in PSP and AD, Acta Neuropathol., 143, 225, 10.1007/s00401-021-02392-2 · DOI
  42. Bright, 2019, Neuroinflammation in frontotemporal dementia, Nat. Rev. Neurol., 15, 540, 10.1038/s41582-019-0231-z · DOI · Paper page
  43. Alster, 2020, Microglial Activation and Inflammation as a Factor in the Pathogenesis of Progressive Supranuclear Palsy (PSP), Front. Neurosci., 14, 893, 10.3389/fnins.2020.00893 · DOI
  44. Panda, 2003, Differential regulation of microtubule dynamics by three- and four-repeat tau: Implications for the onset of neurodegenerative disease, Proc. Natl. Acad. Sci. USA, 100, 9548, 10.1073/pnas.1633508100 · DOI · Paper page
  45. Bachmann, 2021, Differential Effects of the Six Human TAU Isoforms: Somatic Retention of 2N-TAU and Increased Microtubule Number Induced by 4R-TAU, Front. Neurosci., 15, 643115, 10.3389/fnins.2021.643115 · DOI
  46. Barron, 2020, Increasing Tau 4R Tau Levels Exacerbates Hippocampal Tau Hyperphosphorylation in the hTau Model of Tauopathy but Also Tau Dephosphorylation Following Acute Systemic Inflammation, Front. Immunol., 11, 10.3389/fimmu.2020.00293 · DOI
  47. Tuerde, 2018, Isoform-independent and-dependent phosphorylation of microtubule-associated protein tau in mouse brain during postnatal development, J. Biol. Chem., 293, 1781, 10.1074/jbc.M117.798918 · DOI
  48. Sealey, 2017, Distinct phenotypes of three-repeat and four-repeat human tau in a transgenic model of tauopathy, Neurobiol. Dis., 105, 74, 10.1016/j.nbd.2017.05.003 · DOI
  49. Kammenga, 2017, The background puzzle: how identical mutations in the same gene lead to different disease symptoms, FEBS J., 284, 3362, 10.1111/febs.14080 · DOI
  50. Chandler, 2013, Does your gene need a background check? How genetic background impacts the analysis of mutations, genes, and evolution, Trends Genet., 29, 358, 10.1016/j.tig.2013.01.009 · DOI
  51. Hutton, 1998, Association of missense and 5’ -splice-site mutations in tau with the inherited dementia FTDP-17, Nature, 393, 702, 10.1038/31508 · DOI · Paper page
  52. Yoshida, 1993, τ in Paired Helical Filaments Is Functionally Distinct from Fetal τ: Assembly Incompetence of Paired Helical Filament-τ, J. Neurochem., 61, 1183, 10.1111/j.1471-4159.1993.tb03642.x · DOI
  53. Chen, 2010, MAPT isoforms: differential transcriptional profiles related to 3R and 4R splice variants, J. Alzheimers Dis., 22, 1313, 10.3233/JAD-2010-101155 · DOI
  54. Hoover, 2010, Tau mislocalization to dendritic spines mediates synaptic dysfunction independently of neurodegeneration, Neuron, 68, 1067, 10.1016/j.neuron.2010.11.030 · DOI · Paper page
  55. Hori, 2022, Microtubule assembly by tau impairs endocytosis and neurotransmission via dynamin sequestration in Alzheimer ’ s disease synapse model, Elife, 11, 735422, 10.7554/eLife.73542 · DOI
  56. Zhou, 2017, Tau association with synaptic vesicles causes presynaptic dysfunction, Nat. Commun., 8, 15295, 10.1038/ncomms15295 · DOI · Paper page
  57. Regan, 2021, Regulation of synapse weakening through interactions of the microtubule associated protein tau with pacsin1, J. Neurosci., 41, 7162, 10.1523/JNEUROSCI.3129-20.2021 · DOI
  58. Soto-Heredero, 2020, Glycolysis – a key player in the inflammatory response, FEBS J., 287, 3350, 10.1111/febs.15327 · DOI
  59. Palmer, 2018, Astrocytes and aging, Front. Aging Neurosci., 10, 1, 10.3389/fnagi.2018.00337 · DOI
  60. O’Sullivan, 2018, Sphingosine 1-phosphate receptors regulate TLR4-induced CXCL5 release from astrocytes and microglia, J. Neurochem., 144, 736, 10.1111/jnc.14313 · DOI
  61. Cherry, 2022, Neuroimmune proteins can differentiate between tauopathies, J. Neuroinflammation, 19, 278, 10.1186/s12974-022-02640-6 · DOI
  62. Gaetani, 2021, Neuroinflammation and alzheimer’s disease: A machine learning approach to csf proteomics, Cells, 10, 10.3390/cells10081930 · DOI
  63. Reid, 2020, Astrocytes in Tauopathies, Front. Neurol., 11, 1, 10.3389/fneur.2020.572850 · DOI
  64. Setó-Salvia, 2022, Elevated 4R-tau in astrocytes from asymptomatic carriers of the MAPT 10+16 intronic mutation, J. Cell Mol. Med., 26, 1327, 10.1111/jcmm.17136 · DOI
  65. Fischer, 2022, Evolutionary perspective of Big tau structure: 4a exon variants of MAPT, Front. Mol. Neurosci., 15, 1019999, 10.3389/fnmol.2022.1019999 · DOI
  66. Kalmár, 2001, Cultured astrocytes react to LPS with increased cyclooxygenase activity and phagocytosis, Neurochem. Int., 38, 453, 10.1016/S0197-0186(00)00090-5 · DOI
  67. Leyns, 2017, Glial contributions to neurodegeneration in tauopathies, Mol. Neurodegener., 12, 50, 10.1186/s13024-017-0192-x · DOI · Paper page
  68. Ran, 2013, Genome engineering using the CRISPR-Cas9 system, Nat. Protoc., 8, 2281, 10.1038/nprot.2013.143 · DOI · Paper page
  69. Dobin, 2013, STAR: Ultrafast universal RNA-seq aligner, Bioinformatics, 29, 15, 10.1093/bioinformatics/bts635 · DOI · Paper page
  70. Katz, 2010, Analysis and design of RNA sequencing experiments for identifying isoform regulation, Nat. Methods, 7, 1009, 10.1038/nmeth.1528 · DOI · Paper page
  71. Wu, 2005, Sequence analysis GMAP : a genomic mapping and alignment program for mRNA and EST sequences, Bioinformatics, 21, 1859, 10.1093/bioinformatics/bti310 · DOI · Paper page
  72. Schneider, 2012, NIH Image to ImageJ: 25 years of image analysis, Nat. Methods, 9, 671, 10.1038/nmeth.2089 · DOI · Paper page
  73. Lisowiec, 2015, Structural determinants for alternative splicing regulation of the MAPT pre-mRNA, RNA Biol., 12, 330, 10.1080/15476286.2015.1017214 · DOI
  74. Purcell, 2007, PLINK: A Tool Set for Whole-Genome Association and Population-Based Linkage Analyses, Am. J. Hum. Genet., 81, 559, 10.1086/519795 · DOI · Paper page
  75. Chang, 2015, Second-generation PLINK: Rising to the challenge of larger and richer datasets, GigaScience, 4, 1, 10.1186/s13742-015-0047-8 · DOI · Paper page
  76. Das, 2016, Next-generation genotype imputation service and methods, Nat. Genet., 48, 1284, 10.1038/ng.3656 · DOI · Paper page
  77. Bowles, 2019, Reduced variability of neural progenitor cells and improved purity of neuronal cultures using magnetic activated cell sorting, PLoS One, 14, 1, 10.1371/journal.pone.0213374 · DOI · Paper page
  78. Liao, 2013, The Subread aligner : fast , accurate and scalable read mapping by seed-and-vote, Nucleic Acids Res., 41, e108, 10.1093/nar/gkt214 · DOI · Paper page

Cited by

Sorted by citations

Metadata

Authors
Bowles, K. R., Pedicone, C., Pugh, D. A., Oja, L.-M., Sousa, F. H., Keavey, L. K., Fulton-Howard, B., Weitzman, S. A., Liu, Y., Chen, J. L., Disney, M. D., & Goate, A. M.
Venue
Cell Reports
Publisher
Elsevier BV
Published
2024-12
Volume
43
Issue
12
Pages
115013
ISSN
2211-1247
DOI
10.1016/j.celrep.2024.115013
PMC
PMC13478741
Cited by
20
References
18
Language
en
Licence
Funders
  • Curepsp
  • Tau Consortium
  • National Center for Advancing Translational Sciences (U01 AG045390)
  • BrightFocus Foundation
  • UK Dementia Research Institute (UKDRI-4015)
  • Association for Frontotemporal Degeneration
  • Icahn School of Medicine at Mount Sinai
  • National Institute on Aging
  • Rainwater Charitable Foundation
  • Medical Research Council
  • National Institute of Neurological Disorders and Stroke (U54 NS092089)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review